Connective tissue, its cells and extracellular matrix, determines the mechanical and many of the physiologic properties of lung tissue. Inflammation in lung leads to formation of new connective tissue, destruction of normal lung architecture and reduced pulmonary function. While it is known that connective tissue cells form the various ground substance glycosaminoglycans and the associated fibrous proteins of the connective tissue, it is not known how the various pulmonary cell types interact to promote the inflammatory process. Mediators of inflammation which generate and support pulmonary inflammation are poorly understood, at best. The present proposal utilizes essentially homogeneous pig lung connective tissue cells to measure the ability of defined cell populations to synthesize glycosaminoglycans and collagen. In addition, we would define factors regulating the phagocytic capability of lung cells. It will be important to identify and characterize intra and extrapulmonary polypeptide mediators which may be important in regulating connective tissue formation and phagocytosis during pulmonary inflammation. These studies will include definition of the molecular mechanisms by which such factors control selected components of the inflammatory response. Lastly, the present investigation will conclude with studies on cells derived from lungs exhibiting acute and chronic inflammation, examining the same parameters employed for normal lung. This information would be correlated with both morphologic and physiologic changes found in pathologic lung tissue and should help highlight the central control mechanisms in pulmonary inflammation.